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161 Cards in this Set
- Front
- Back
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psychosis
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disordered though process
acute v chronic (more common) |
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hallucination
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sensory perception of people or objects that arent present
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delusions
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false belief without reason or evidence
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schizophrenia
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chronic
variety of related disorders -dopa/seratonin system high levels of both = psychosis |
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antipsychotic drugs prototype
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thorazine
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how is thorazine well absorbed
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PO and perentally
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thorazine mechanism of action
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occupy or block dopamine receptors
-increased dopa = psychosis |
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uses of thorazine
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schizophrenia
anti-emetic intractable hiccups hyperarousal states: ADD, insomnia, acute freak outs |
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dependence with thorazine
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no physical or psychological dependence
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pt teaching for thorazine
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takes awhile to build blood levels to be effective
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reasons for long term thorazine use
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head traumas tx
brain tumor ETOH withdrawal stroke ...because dopa is affected by these |
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ADEs of thorazine...specifically ANS and CNS
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ANS Depressent
-Antiadrenergic: blocks SNS, severe fatigue, decreased BP and HR, bronchoconstriction, ortho hypoTN -Anticholinergic: blocks PSNS, DRY, blurred vision, tachycardia, decreased UO **CNS depressant too |
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extra pyramidal effects/ADE of thorazine
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1. dyskinesia: rhythmic invol movements
2. dystonia: rigid, back and neck, pulls head 3. pseudo parkinsons: pill rolling, shuffle gate 4. tardive dyskinesia: chronic, invol jerky movements of face...tongue in and out fast and puffing cheeks **these effects can be permanent |
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treatment for extrapyramidal effects
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decrease the dose can help
-treat with anticholinergic drug too or benadryl...3 mos will decrease s/s |
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ADE hemolytic anemia from what and what is it
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thorazine ADE
-breakup RBCs, increases bilirubin and you get jaundice |
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contraindications for antipsychotic drugs/thorazine
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-liver damage
-CAD: tachy and bradycardia risk -Parkinsons -Cautious w/ seizures, lung/resp disorders -pregnant or lactating |
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Eval for antipsychotics...s/s you might see
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-ineffective individual coping
-potential for injury: hemo anemia, ADE -decreased CO -impaired physical mobility -altered thought processes..Tx to dec hallucinations -sensory perceptual alterations (tx) -activity intolerance (drowsy) |
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thorazine interventions
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1. allergies
2. hepatic disease 3. administer w/ food 4. BP swings 5. avoid skin contact...burns, change needle 6. don't mix with ETOH or other narcotics 6. |
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pt education for thorazine
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avoid driving and using heavy machinery because of drowziness
-take before bed bc sedative (1hr) -postural hypoTN, change position gradually |
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tx time for thorazine
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a year to life
...can take weeks or months to see results |
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toxic OD with thorazine
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don't induce vomitting
might not be able to turn head with dystonia so NG levage |
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what happens if pts BP drops and bradycardia with thorazine
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lethal to use Epi
will bottom out BP and cardiac arrest will occur |
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foods with tyramine
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aged(cheese, wine, beer, yog, SC)
pickled smoked meats caffeine |
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antipsychotic 1st drug of choice
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atypical or non-phenothiazines
-very few ADE compared so more compliance |
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atypical or non-phenothiazine prototype
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clozaril
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ADE of clozaril
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-agranulocytosis: Do Composite Blood count
-increased blood sugar: so high that black box warning for phenoketoacidotic coma -fewer acute episodes and hospitalizations |
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etiology of depression symptoms
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-neurotransmitter abnormalities or with receptors
-genetics -endocrine factors |
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APA of depression
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1. major depression: mood + 5 s/s from list
2. dysthymia: lack of rhythm, -primary: no ID'ed cause -secondary: related to envt stresses or life events, meds (ETOH, HTN, roids, BCPS) and concurrent physical diseases |
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antidepressant drug groups
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1. MAOI's
2. tricyclic antidepressants 3. lithium 4. selective serotonin reuptake inhibitors |
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MAOI defintion and prototype
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monoamine oxidase inhibitors
Marplan |
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MAOI actions
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enzymes decrease metabolism of neurotransmitters at receptor sites so NorEpi and Dopa increase
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onset of MAOI
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1-2 weeks
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ADE of MAOIs
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orthostatic HTN
impotence sedation/insomnia HTN crises*** paresthesias: numbness/tingling of hands and feet anticholinergic: DRY |
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HTN crises and MAOIs
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watch for increased BP
any OTC cough meds, MSG and asthma can increase -tyramine in foods is precursor to NorEpi in GI and small amounts are absorbed and MAOIs block this, gets absorbed in high quantities -increases in NorEpi to cause MI, cerebral bleeds and headaches |
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TCA prototype
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elavil
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action of TCAs
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block reabsorption so increases in NorEpi, Seratonin and Dopa occur
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onset of TCAs
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10-30 days
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ADE of TCAs
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orthostatic HTN
dysrhythmias impotence leukopenia sedation anticholinergic -may be given with MAOI |
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what can TCAs be used to treat
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bulimia
phobias neurogenic pain |
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lithium tx for
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bulimia
bipolar disorders cluster headaches |
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onset of lithium
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6 days
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metabolism of lithium
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not metab, excreted soley by kidneys
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ADE of lithium
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weight gain
GI: upset, n/v, METALLIC taste Tremors: ataxia Polyuria and dipsia Leukocytosis (inc WBC) Na imbalances |
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explain Na imbalance prob with Lithium
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watch dietary shifts
-lithium reabsorption = dec Na inverse relationship |
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SSRI prototype
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prozac
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1st drug of choice for depression
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SSRI
prozac -no more effective just fewer ADE so increased compliance because 1x/day dose |
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ADE of SSRIs
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skin rash
GI (anorexia, wt loss, N/V) stimulant: anxiety, nervousness |
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SSRIs can also be used to treat
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bulimia
OCD |
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suicide rates and antidepressants
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same suicide rates
-small %, less than 3, have violent/suicidal thoughts in first few weeks |
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antidepressant summary
-onset and other info |
2-4 weeks
-significant 1st pass effect -interact with many other drugs |
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antidepressants pre-op
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taper dose and d/c 1 week pre-op
-resume when pt is taking PO fluid and food |
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NSSRI (norepi selective seratonin reuptake inhibitor)
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block reuptake of NorEpi and seratonin
-prob is that NorEpi is a potent vasoconstrictor = increased BP -So HTN pts may not be candidates |
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antidepressant pt teaching
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-avoid hazardous activity
-avoid alcohol bc of sedation/depress -compliance w/ therapy...weeks -check prior to taking OTC meds -medic alert bracelet: long term 1st 3 -foods to avoid (tyramine MAOI) -avoid sudden position changes -avoid caffeine(MAOI) -use sugarless gum/candy because of antichol effect -don't alter Na intake -report skin rash...esp SSRI |
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prob if pt has glaucoma on antidep
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anticholinergic effect would increase pressure
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seizure
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abnormal electrical activity
OD on meds severe hypoglycemia can be single event like high fever ETOH withdrawal and abuse |
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convulsion
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tonic (sustained contractions) clonic (jerking) seizures
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epilepsy
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s/s of seizure activity
abnormal EEG |
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status epilepticus
#1 cause too |
one seizure after another w/o gaining consciousness
-#1 cause = stopping meds |
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causes of status epilepticus
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brain tumor
neuro trauma ETOH withdrawal stopping meds -may be spike in BP and then it falls |
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effects of status epilepticus
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tonic clonic movements impede teh thorax
-hypoxia and brain damage |
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post ictal state
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breathingm may be semi-responsive
put in rescue position on their side |
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tx for status ep
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oxygen
IV fluids protect use benzodiazapine to break (long lastingO) not long term tx |
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antiseizure AEDs mechanism of action
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1. block movement of Na into nerve cell: increase threshold of seizure activity, required for normal conduction = dec responsiveness to stimuli
2. enhance the activity of GABA: neurotrans in brain, benzodiaz are GABA enhancers, increases ability to inhibit seizures and will have fewer |
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antiseizure AED prototype
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dilantin
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ADE of dilantin/antiseizure meds
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CNS: ataxia. lethargy
GI N/V Gingival hyperplasia |
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1st drug of choice for antiseizures and how it's given
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dilantin
IV: mix only with saline solution...dextrose will ppt it |
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therapeutic use of antiseizure meds
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seizures
prevent w/ neurosurgery severe brain injury nerve pain treatment(tegretol, klonopin) |
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questions to ask with antisezures meds
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are you using to treat or prevent (b4 brain surgery)?
have you had seizures before? how often? how long since your last? does anything ppt your seizure? |
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phenobarb use as antiseizure/AED med
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long acting barbiuitate
prevention animal hospitals to inc appetite ADE= CNS depressant |
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contraindications for antiseizure meds
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cns depressant use
allergies |
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PT eval for antiseizure meds
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risk for injury: tonic/clonic, etc
noncompliance (status) |
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DM
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chronic systemic disease of abnormalities
-Metabolic: changes in metab of CHO, fats, pro = inc BS -Vascular: atherosclerosis, changes in microcirc |
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goals of DM drug therapy
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BS of 70-110
-prevent complications -prevent hypoglycemia |
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diff between type I and II
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type I is
-early onset - sudden -tends to be harder to control, -destroys B-cells, -autoimmine - higher rate of complications -insulin needed v oral hypoglycs -no insulin production v decrease prod or resistance |
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s/s of DM
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polyuria...kidneys dump in gluc
polydipsia polyphagia...hungry, cells don't get nutrients |
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when would you need insulin for type II diabetes
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stress, trauma from hospital, surgery
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tx for hyperkalemia with diabetcis
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give dextrose and insulin
-force K intracellularly until better treatment can be given ER measure |
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hypoglycemia response
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SNS response
palpitations clammy sweat tremors confused irritable |
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insulin impt info in general
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-rapid and short acting insulin covers meals immediately AFTER the injection
-intermediate acting insulin is expected to cover subsequent meals -long acting insulin provides a relatively constant level of insulin and act as a basal insulin |
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only what type of insulin is given IV
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regular but can also be given subQ before meals
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conventional insulin regime
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1-2 injections/day, BS WNL
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intensive insulin regime
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many injections daily
keep tight control of BS -test BS as many times as you inject a day |
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oral agents for impaired insulin productions
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oral hypoglycemics
-stimulate the production of insulin -sulfonylureas: (glucotrol) -meglitinidines: prandin -decrease BS by increasing insulin secretion...need fxning B cells |
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oral agents for insulin resistance
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a decreased sensitivity of the tissues to insulin
-Thiazolidines: actos -Diguanide: glucophage -oral alpha glucosidase inhibitors (glyset) |
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using insulin in icu
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for non-diabetics
-keep BS normal, heal faster and decrease complications |
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prototype of sulfonylureas
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glucotrol
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primary and secondary failure with oral agents
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primary: stops working, no reason
secondary: pt was non-compliant |
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contraindications for oral hypoglycemics
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fetal hypoglycemia
death |
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hormones produced by the thyroid
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1. thyroxine (T4)
2. triiodothyronine (T3) 3. calcitonin: released when Ca increases in body (>10) |
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signif with glucophage
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not metab by liver
excreted unchanged in urine |
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contraindications for glucophage
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renal fxn and death
stop 48 hours before a test with contrast dye |
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fxn of thryoid hormones
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controls cellular metabolism
-required for growth and development |
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thyroid disorders
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1. goiter: I deficiency
2. hypothyroidism: synthroid |
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cretinism
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congenital hypothyroid in kids
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hypothyroidism
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dec BMR and BP
bradycarida lethargy, apathy, drowsy slow speech and mental dullness wt gain, intolerant to cold dysmennorhea and infertility |
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synthroid action
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increases BMR
acts on thyroid on it for life |
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hyperthyroid prototype
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tapazole
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other meds for hyperthyroidism besides tapazole
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saturated soln of K Iodide (SSKI): stops release of hormones
Lugol's pre op use sometimes |
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synthroid pt teaching
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3-7 days to see effects
may need to increase dose take as directed same time each day pulse |
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hyperthyroid s/s
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increased BMR, HR, MP
palpitations anxious protruding eyeballs |
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contraindicatiosn for hyperthyroid meds
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preg or nursing mom because of cretinism
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adrenal cortex produces
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1. adrenal sex hormones
2. mineral corticoids 3. glucocorticoids |
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mineral coritcoids
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aldosterone: decreases = Addisons Disease w/ dec Na and H20 and inc K
increases=cushings disease opposite -holds water and Na to kidneys-i -increased BP...hypokalemia FLUID AND ELECTROLYTE BALANCE |
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actioins of glucocorticoids (steroids)
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1. CHO Metab: stim formation of gluc, make cells insulin resistance, inc BS
2. Inflamm/Immune System: suppression 3. Nervous Syst: dec excitability, slow cereb/cortex, euphoria to psychosis, changes mood, brain wave 4. GI: dec viscosity, mucous layer and inc HCL 5. Pro metab: inc breakdown, and pro synthesis rate 6. fluid/electrolyte: retain Na/H20...kidney rides Ca/K, hypokalemia, edema, HTN, osteo 7. Resp Syst: more resp to bronchodil, stabilize mast cells, dec histamine released |
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ADE long term steroid use
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muscle wasting
buffalo hump round face skinny arms and legs |
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replacement therapy and roids
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small dosees
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therapeutic use of steroids
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larger doses
extension of physiological effects doesn't cure |
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to decrease ADEs of steroids you should
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1. local use
2. short course 3. taper dose 4. ADT or double dose every other day |
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steroid prototype
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prednisone
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antiinflamm roid med
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prednisone
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neuro roid med
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decadron
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allergic disorders med roid
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medrol
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endocrine disroders roid med
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cortisone
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GI roid med and immunosuppressant
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prednisonea
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avoid use or use roids cautiously in
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-those at risk or with infection
-DM -Peptic ulcer disease -inc BP and CHF -Renal insufficiency -Psychosis |
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contraindciations for roids
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systemic fungal infection
TB |
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assess what with roid use
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BP
electrolytes BS I &O weight growth in kids occult blood edema T stress level |
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interventions for roids
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Maintenance: ADT
give before 9 am give with milk or food taper pt education |
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peptic ulcer disease
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areas exposed to HCL, pepsin
-lower esoph,stomach,duodenum -initially irritation, then more inflamm and it erodes and becomes an ulcer |
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causes of GERD
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stress meds
h, pylori |
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cell protection in GI
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mucus
dilution of HCL tight cardiac sphincter cytoprotective prostaglandins alkalinization |
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cell destruction in GI casues
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HCl: acetylcholine (wet, increase motility and digestion, hist II rleases HCl too
-pepsin from chief cells (ph<3) -h. pylori |
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types of anti-ulcer meds
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1. antacids
2. ulcer adherent 3. histamine 2 receptor blockers 4. proton pump inhibitors 5. H. pylori agents |
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antacid meds for GI
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1. Al hydroxide: amphogel
2. Mg: MOM 3. Al & Mg: maalox 4. Na Bicarbonate: alka seltzer 5. Ca Carbonate: Tums |
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what GI drugs constipate
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anything with aluminum
-amphogel |
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signif about calcium carbonate (tums)
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acid rebound when you stop taking them and it can make it worst
- wouldn't use to treat gastric ulcer |
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signif of Na bicarb (alka seltzer)
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increase in Na so beware with HTN or Na restricted diets
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therapeutic effects of antacids
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chemical neutralization
decreases pain, burning type |
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assessment for antacids
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taking other meds? that might interfere with absorption
-na restricted? bowel fxn? |
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interventions with antacids
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shake
water full glass or you'll only coat esoph) not with other meds 1 hour after meals |
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ulcer adherent propotype
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sucralfate
carafate |
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ADES of ulcer adherents/sucralfate
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Nausea
constipation metallic taste dry mouth |
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ulcer adherent info...uses etc, how its taken
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-prevents and treats
-cumbersome schedule: 1-2 hrs ac and hs for 4-8 wks -only local action -on empty stomach and again at bed |
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histamine 2 receptor blockign agents prototype
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tagamet
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mechanism of His II blockers
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stop production and release of His II which decreases the release of HCl
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histamine effects I and II
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H I: bronchoconstriction, edema, redness, pain, tingle, itch..released with asthma, allergies, tissue injury
HII: INCREASE HCl production, only in GI, strong stim, PSNS (vagus, acetylcholine released) |
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his II uses, how its given etc
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-prevents and treats ulcers (PUD)
-6-8 wks for ulcer to heal |
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issue with tagamet
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interferes with metabolism of many drugs
-mental confusion in elderly |
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assessment for His II receptor blocking agents
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-renal fxn
-liver fxn -other meds -allergies -preg/lactating bc it crosses placenta -not recommended for kids |
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interventions for His II receptor blocking agents (tagamet)
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-can give w/o regard to meals
-quit smoking and dec HCl made -assess for ADES (rare N, diarrhea) -stress |
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proton pump inhibitor prototype
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prilosec
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1st drug of choice with GI
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prilosec as logn as not allergy
more effective then his II |
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mechanism of proton pump inhib
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prevents or stops the release of gatric acid
given PO or IV |
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ADES of prilosec
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minimal
-N, D, headache |
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H. pylori agents...describe
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combo of:
1. antibiotic: 2 of 4 -amoxicillin -biaxin -flagyl -tetracycline 2. pro pump inhib: prevacid or H2 blocker |
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previpak
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1 prevacid
2 amox 1 biaxin - -2 weeks of treatment |
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causes of diarrhea
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excess lax use
spicy foods IBS/crohns intestinal cancers |
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non-specific therapy for anti-diarrheals
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-opiate derivatives: cause?
demerol, paragoric -misc: pepto, kaopectate -anticholinergics: lomotil and narcotic |
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how to describe diarrhea
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-acute/chronic
-mild/severe -self limiting: subsides in 24-48 hrs |
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specific diarrhea therapy
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antibiotics
digestive enzymes |
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assessment for anti-diarrheals
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# of stools, looseness
I & O skin turgor weight |
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PT Eval with anti diarrheals
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altered nutrition
social isolation FVD pain |
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interventions for anti-diarrheals
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-ID cause
-increase fluid intake -hand washing -BRAT diet (ban, rice, applesauce, toast/tea) -avoid irrit foods -probiotics |
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anti emetics for GI
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1. phenothiazines
2. antihistamines: give ahead, drama 3. seratonin receptor antagonists: zofran for chemo N/V give IV before 4. benzodiazapines: not anti-emetic...multi drug regime because it promotes sedation, relax to dec n/v |
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uses of anabolic androgen steroids AAS
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stimulation of:
-bone marrow -sexual development -palliative tx -tx of tissue wasting (breast cancer, AIDS, ESRD) |
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2 types of AAS
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1. oil based
2. water based: carry more ADE, clear body within 1-2 days |
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ADES of AAS
REVERSIBLE |
1. acne
2. aggression 3. HTN 4. sterility (atrophy of testes) 5. dysuria: esp males prostate enlarges |
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Irreversible ADES of AAS
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1. impotence
2. baldness 3. gynocomastia (breasts) 4. stunted growth 5. psych changes 6. enlarged clitoris 7. disrupt mesnes |
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pathophys ADES of AAS
(cells etc) |
-destroys liver cells
-liver cancer -heart disease -inc blood clotting -psych changes (superman complex too) |
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other drug use in sports
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-HGH
-blood transfusions at high elevations -brake drugs: stop estrogen in girls to delay puberty -beta blockers: for aim -diuretics : wt sports, lose K issue |
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withdrawal of AAS
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depression
weaker lethargic lose muscle mass turn to other drugs |
